Accumulating evidence demonstrates that breathing air pollutants leads to devastating increases in sickness and death worldwide over time. However, there is little data comparing the effects of different types of air pollution on health. In Canada, traffic-related air pollution and wood smoke (wildfires and wood burning for heating) are very common air pollutants. This study aims to safely complete a controlled human exposure study to test how these air pollution types acutely affect health.
Healthy adult participants (total 48; 24 of each biological sex assigned at birth) will breathe filtered air (control), wood smoke (WS), diesel exhaust (DE), and DE plus WS (DEWS) each for 2 hours, with 4 weeks between each exposure (washout). Before and after each exposure, participants will answer questions, perform breathing tests, and give blood samples. At 24 hours after each exposure, participants will undergo a bronchoscopy to collect samples from their lungs. The study will look at what (if any) are the differences between breathing in fresh air (filtered air - FA) or polluted air containing either wood smoke (WS), diesel exhaust (DE) or diesel exhaust plus wood smoke (DEWS). The research team will use wood smoke generated from pine wood, since it is one of the most common types of wood found in Western Canadian forests where forest fires occur. The investigators will evaluate multiple endpoints as detailed in the Outcome Measures section. For each applicable endpoint, the investigators will evaluate stratified analyses and effect modification by biological sex, participant age, gene score, and microbiomes.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
BASIC_SCIENCE
Masking
TRIPLE
Enrollment
48
Exposure to HEPA filtered air, as a control
Wood smoke (WS) standardized to 300µg/m³ of particulate matter with a diameter of 2.5 micrometers or less (PM2.5).
Diesel exhaust (DE) standardized to 300µg/m³ of particulate matter with a diameter of 2.5 micrometers or less (PM2.5).
Combined diesel exhaust and wood smoke standardized to 300µg/m³ of particulate matter with a diameter of 2.5 micrometers or less (PM2.5).
University of British Columbia
Vancouver, British Columbia, Canada
Woodsmoke (WS) and/or diesel exhaust (DE) exposure effects on inflammatory cells in the lungs.
Differentially count lung cells.
Time frame: Comparison of the different arms (over the span of ~5 months).
Within-individual change in lung transcriptomic biomarkers of inflammation following exposure to woodsmoke and/or diesel exhaust.
Within-individual change in lung biomarkers of inflammation (serum amyloid A (SAA), c-reactive protein (CRP), chemokine ligand 18 (CCL18), and fibrinogen) in RNA.
Time frame: Through study completion, anticipated ~5 months.
Within-individual change in lung protein biomarkers of inflammation following exposure to woodsmoke and/or diesel exhaust.
Within-individual change in lung biomarkers of inflammation (serum amyloid A (SAA), c-reactive protein (CRP), chemokine ligand 18 (CCL18), and fibrinogen) in protein.
Time frame: Through study completion, anticipated ~5 months.
Within-individual change in circulating transcriptomic biomarkers of inflammation following exposure to woodsmoke and/or diesel exhaust.
Within-individual change in circulating biomarkers of inflammation (CX3CL1, CCL23, CXCL8, SAA, MMP9, MMP12, APOB, APOM, SOD1, NQO1, HMOX1, CAT, CYP1B1, CYP1A2, NFE2L2 and AHRR) in RNA.
Time frame: Through study completion, anticipated ~5 months.
Within-individual change in circulating protein biomarkers of inflammation following exposure to woodsmoke and/or diesel exhaust.
Within-individual change in circulating protein biomarkers of inflammation (CX3CL1, CCL23, CXCL8, SAA, MMP9, MMP12, APOB, APOM, SOD1, NQO1, HMOX1, CAT, CYP1B1, CYP1A2, NFE2L2 and AHRR).
Time frame: Through study completion, anticipated ~5 months.
Within-individual change in airway resistance following exposures to woodsmoke and/or diesel exhaust.
Within-individual change in airway resistance, as measured by impulse oscillometry (resonant frequency (Fres) and peripheral airway resistance (R5-R20)) across exposures to woodsmoke and/or diesel exhaust relative to filtered air.
Time frame: Through study completion, anticipated ~5 months.
Woodsmoke (WS) and/or diesel exhaust (DE) exposure effects on inflammatory cells in the nose.
Differentially count nasal cells.
Time frame: Comparison of the different arms (over the span of ~5 months).
Within-individual changes in exhaled nitric oxide following woodsmoke (WS) and/or diesel exhaust (DE) exposures.
Measurement of fractional exhaled nitric oxide (FeNO) in parts per billion (ppb).
Time frame: Comparison of the different arms (over the span of ~5 months).
Woodsmoke (WS) and/or diesel exhaust (DE) exposure effects on symptoms, stress and perceptions.
Visual analog score (0-100) questionnaire will be completed, with a higher score indicating a worse outcome.
Time frame: Comparison of the different arms (over the span of ~5 months).
Woodsmoke (WS) and/or diesel exhaust (DE) exposure effects on lung function.
Lung function as evaluated by spirometry (e.g. FEV1).
Time frame: Comparison of the different arms (over the span of ~5 months).
Woodsmoke (WS) and/or diesel exhaust (DE) exposure effects on nasal resistance.
Measurement of peak nasal inspiratory flow (PNIF).
Time frame: Comparison of the different arms (over the span of ~5 months).
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